The metabolic syndrome is characterised by an increased amount of adipose tissue inside the abdominal cavity (popularly called belly fatness), insulin resistance with increased risk of developing senile diabetes, i.e. diabetes type II (=NIDDM, non-insulin dependent diabetes mellitus), high levels of blood fats and high blood pressure. Parallel to this is an increased risk of coronary, apoplexy, sudden death and other arteriosclerotic conditions.
A hypothetical explanation to the metabolic syndrome could be an overproduction of cortisol, a stress hormone which causes an accumulation of fat inside the abdominal cavity, and insulin resistance. Theoretically this could, through secondary metabolic effects, explain the other disorders related to the metabolic syndrome.
In Metabolism, vol. 41, No 8, 1992, pages 882–886, is shown that belly fat women have higher secretion of cortisol than “evenly fat” women. The same work describes the effects of acute mental stress on the production of cortisol. It was shown that belly fat women, at a given stress signal, produced more cortisol than ‘evenly fat’ women. This suggested, but did not prove, that there may be a relationship between stress and belly obesity. A dexamethasone inhibitor test was carried out with 1 mg dexamethasone and subsequent measurement of cortisol content in serum. No difference in inhibitory effect on the production of cortisol could be found between the groups of belly fat women and to evenly fat women and standard values.
Cortisol analogues, e.g. dexamethasone, have for many years been used to track so called endogenous (often hereditary) depressions in humans. The mechanism behind the test is however so far unknown.